Search results for "FMS"

showing 10 items of 44 documents

Clinical resistance to the kinase inhibitor PKC412 in acute myeloid leukemia by mutation of Asn-676 in the FLT3 tyrosine kinase domain.

2005

Activating mutations in the FLT3 tyrosine kinase (TK) occur in approximately 35% of patients with acute myeloid leukemia (AML). Therefore, targeting mutated FLT3 is an attractive therapeutic strategy, and early clinical trials testing FLT3 TK inhibitors (TKI) showed measurable clinical responses. Most of these responses were transient; however, in a subset of patients blast recurrence was preceded by an interval of prolonged remission. The etiology of clinical resistance to FLT3-TKI in AML is unclear but is of major significance for the development of future therapeutic strategies. We searched for mechanisms of resistance in 6 patients with AML who had relapses upon PKC412 treatment. In an …

ImmunologyMutation MissenseBiologyBiochemistrychemistry.chemical_compoundIn vivoRecurrencehemic and lymphatic diseasesHumansProtein Kinase InhibitorsProtein Kinase CQuizartinibKinaseMyeloid leukemiaCell BiologyHematologyProtein-Tyrosine KinasesStaurosporineEnzyme ActivationProtein kinase domainchemistryfms-Like Tyrosine Kinase 3Drug Resistance NeoplasmLeukemia MyeloidFms-Like Tyrosine Kinase 3Acute DiseaseCancer researchTyrosine kinaseCrenolanibBlood
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A novel molecular mechanism of primary resistance to FLT3-kinase inhibitors in AML

2009

Abstract Currently, FLT3 tyrosine kinase inhibitors (TKIs) are emerging as the most promising drug therapy to overcome the dismal prognosis of acute myelogenous leukemia (AML) patients harboring internal tandem duplications (ITDs) of FLT3. However, up-front drug resistance occurs in approximately 30% of patients, and molecular mechanisms of resistance are poorly understood. Here, we have uncovered a novel mechanism of primary resistance to FLT3 TKIs in AML: an FLT3 receptor harboring a nonjuxtamembrane ITD atypically integrating into the β-2 sheet of the first kinase domain (FLT3_ITD627E) induces dramatic up-regulation of the anti-apoptotic myeloid cell leukemia 1 protein (MCL-1). Using RNA…

KinaseMitogen-Activated Protein Kinase 3ImmunologySignal transducing adaptor proteinCell BiologyHematologyBiologyBiochemistryProtein kinase domainhemic and lymphatic diseasesTrk receptorFms-Like Tyrosine Kinase 3Cancer researchSignal transductionTyrosine kinaseBlood
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Dendritic cells in liver injury and fibrosis: shortcomings and promises.

2013

SummaryThe phenotype and function of liver dendritic cells (LDCs) are poorly understood. This Snapshot summarizes our current knowledge on LDCs in the healthy and injured liver, and their role in fibrosis progression and reversal. It also draws attention to various pitfalls in the current experimental design and conclusions based on available data.

Liver CirrhosisLiver dendritic cellsPlasmacytoid dendritic cellBiologyCCL2MiceFMS-like tyrosine kinase 3 ligandFibrosismedicineAnimalsHumansAntigen-presenting cellLiver injuryHepatologyFlt3LDendritic Cellsmedicine.diseaseCD11c-DTRDisease Models Animalmedicine.anatomical_structurePhenotypeLiverImmunologyHepatic stellate cellDisease ProgressionBone marrowToleranceJournal of hepatology
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Bis(1H-indol-2-yl)methanones are effective inhibitors of FLT3-ITD tyrosine kinase and partially overcome resistance to PKC412A in vitro.

2009

Inhibition of the mutated fms-like tyrosine kinase 3 (FLT3) receptor tyrosine kinase is a promising therapeutic strategy in acute myeloid leukaemia (AML). However, development of resistance to FLT3 tyrosine kinase inhibitors (TKI), such as PKC412A, has been described recently. This observation may have an increasing impact on the duration of response and relapse rates in upcoming clinical trials employing FLT3-TKI. Herein we investigated two representatives of a novel class of FLT3-TKI: Bis(1H-indol-2-yl)methanones. Both compounds effectively induced apoptosis in FLT3-internal tandem duplicate (ITD)-transfected murine myeloid cells and in primary FLT3-ITD positive blasts. Combination of bot…

MAPK/ERK pathwayIndolesmedicine.drug_classAntineoplastic AgentsApoptosisTransfectionTyrosine-kinase inhibitorReceptor tyrosine kinaseCell Linefluids and secretionshemic and lymphatic diseasesmedicineTumor Cells CulturedHumansProtein kinase Bbiologyhemic and immune systemsHematologyStaurosporineIn vitroLeukemia Myeloid Acutefms-Like Tyrosine Kinase 3Drug Resistance NeoplasmTandem Repeat SequencesTrk receptorembryonic structuresFms-Like Tyrosine Kinase 3Cancer researchbiology.proteinTyrosine kinasepsychological phenomena and processesBritish journal of haematology
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Prognostic value of FLT3 mutations in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline monochemother…

2011

Background Fms-like tyrosine kinase-3 (FLT3) gene mutations are frequent in acute promyelocytic leukemia but their prognostic value is not well established. Design and Methods We evaluated FLT3-internal tandem duplication and FLT3-D835 mutations in patients treated with all-trans retinoic acid and anthracycline-based chemotherapy enrolled in two subsequent trials of the Programa de Estudio y Tratamiento de las Hemopatias Malignas (PETHEMA) and Hemato-Oncologie voor Volwassenen Nederland (HOVON) groups between 1996 and 2005. Results FLT3-internal tandem duplication and FLT3-D835 mutation status was available for 306 (41%) and 213 (29%) patients, respectively. Sixty-eight (22%) and 20 (9%) pa…

MaleAIDA PROTOCOLGene mutationmedicine.disease_causeGastroenterologyLeukemia Promyelocytic AcuteRESIDUAL DISEASEhemic and lymphatic diseasesMOLECULAR SUBTYPESChildanthracyclinesMutationRemission InductionFLT3 mutationshemic and immune systemsHematologyMiddle AgedPrognosisall-trans retinoic acidLeukemiaTreatment Outcomeembryonic structuresFemaleTandem exon duplicationmedicine.drugAcute promyelocytic leukemiaAdultmedicine.medical_specialtyAdolescentAntineoplastic AgentsTretinoinACUTE MYELOID-LEUKEMIABiologyYoung AdultQUALITY-CONTROLTretinoinPOOR-PROGNOSISInternal medicinemedicineCoagulopathyHumansAgedprognostic factorsOriginal Articlesacute promyelocytic leukemiamedicine.diseaseSurvival AnalysisINTERNAL TANDEM DUPLICATIONRISK-ADAPTED TREATMENTPML/RAR-ALPHAfms-Like Tyrosine Kinase 3Fms-Like Tyrosine Kinase 3ImmunologyPETHEMA GROUPMutation
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Sorafenib in combination with intensive chemotherapy in elderly patients with acute myeloid leukemia : results from a randomized, placebo-controlled …

2013

Purpose The prognosis of elderly patients with acute myeloid leukemia (AML) is still dismal even with intensive chemotherapy. In this trial, we compared the antileukemic activity of standard induction and consolidation therapy with or without the addition of the kinase inhibitor sorafenib in elderly patients with AML. Patients and Methods All patients received standard cytarabine and daunorubicin induction (7+3 regimen) and up to two cycles of intermediate-dose cytarabine consolidation. Two hundred one patients were equally randomly assigned to receive either sorafenib or placebo between the chemotherapy cycles and subsequently for up to 1 year after the beginning of therapy. The primary ob…

MaleNiacinamideSorafenibOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentPlacebo-controlled studyMedizinPlaceboDouble-Blind MethodInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansProtein Kinase InhibitorsAgedAged 80 and overChemotherapybusiness.industryPhenylurea CompoundsConsolidation ChemotherapyMiddle AgedSorafenibSurgeryLeukemia Myeloid AcuteRegimenfms-Like Tyrosine Kinase 3OncologyTolerabilityMutationCytarabineFemalebusinessmedicine.drug
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Influence of molecular subgroups on outcome of acute myeloid leukemia with normal karyotype in 141 patients undergoing salvage allogeneic stem cell t…

2012

Based on molecular aberrations, in particular the NPM1 mutation (NPM1(mut)) and the FLT3 internal tandem duplication (Flt3-ITD), prognostic subgroups have been defined among patients with acute myeloid leukemia with normal karyotype. Whereas these subgroups are known to play an important role in outcome in first complete remission, and also in the indication for allogeneic stem cell transplantation, data are limited on their role after transplantation in advanced disease. To evaluate the role of molecular subgroups of acute myeloid leukemia with normal karyotype after allogeneic stem cell transplantation beyond first complete remission, we analyzed the data from 141 consecutive adults (medi…

MaleOncologyTransplantation Conditioningmedicine.medical_treatmentHematopoietic stem cell transplantation0302 clinical medicineRecurrenceAntineoplastic Combined Chemotherapy ProtocolsHematopoietic Stem Cell TransplantationNuclear ProteinsMyeloid leukemiaInduction ChemotherapyHematologyMiddle Aged3. Good healthFludarabineTreatment OutcomeLeukemia Myeloid030220 oncology & carcinogenesisAcute DiseaseFemaleNucleophosminmedicine.drugAdultmedicine.medical_specialtyAllogeneic transplantationAdolescentPrimary Induction FailureKaryotypeDisease-Free SurvivalYoung Adult03 medical and health sciencesInternal medicinemedicineHumansTransplantation HomologousAgedSalvage Therapybusiness.industryMinimal residual diseaseSurgeryTransplantationfms-Like Tyrosine Kinase 3Multivariate AnalysisMutationTransplantation ConditioningOriginal Articles and Brief ReportsbusinessFollow-Up Studies030215 immunology
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Identification of a novel activating mutation (Y842C) within the activation loop of FLT3 in patients with acute myeloid leukemia (AML).

2004

Fms-like tyrosine kinase 3 (FLT3) receptor mutations as internal tandem duplication (ITD) or within the kinase domain are detected in up to 35% of patients with acute myeloid leukemia (AML). N-benzoyl staurosporine (PKC412), a highly effective inhibitor of mutated FLT3 receptors, has significant antileukemic efficacy in patients with FLT3-mutated AML. Mutation screening of FLT3 exon 20 in AML patients (n = 110) revealed 2 patients with a novel mutation (Y842C) within the highly conserved activation loop of FLT3. FLT3-Y842C-transfected 32D cells showed constitutive FLT3 tyrosine phosphorylation and interleukin 3 (IL-3)-independent growth. Treatment with PKC412 led to inhibition of proliferat…

Models MolecularImmunologyBiologymedicine.disease_causeBiochemistryCell Linechemistry.chemical_compoundMicefluids and secretionshemic and lymphatic diseasesProto-Oncogene ProteinsmedicineSTAT5 Transcription FactorAnimalsHumansTyrosinePhosphotyrosineMutationCell CycleMyeloid leukemiaReceptor Protein-Tyrosine Kinaseshemic and immune systemsTyrosine phosphorylationCell BiologyHematologymedicine.diseaseMilk ProteinsProtein Structure TertiaryDNA-Binding ProteinsEnzyme ActivationLeukemiaLeukemia Myeloid AcutechemistryGene Expression Regulationfms-Like Tyrosine Kinase 3embryonic structuresFms-Like Tyrosine Kinase 3MutationCancer researchTrans-ActivatorsTyrosineSignal transductionTyrosine kinaseSignal TransductionBlood
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Examination of fundamental movement patterns and likelihood of injury in amateur runners from Opole region in Poland

2018

Background: The most common risk factors for running-related injuries are mistakes, such as insufficient warm-up and stretching exercises, during training. Good preparation and proper training reduces the risk of sport-related injuries. Aim of the study: To examine fundamental movement patterns and likelihood of injury in amateur runners. Material and methods: Twenty-four amateur long-distance runners from Opole region (Poland) were divided into two groups. The first group comprised 12 runners from the club “Kotwica Brzeg”, who did a proper warmup before training and stretching exercises after training. The second group comprised 12 runners from other clubs who did not undertake any warm-up…

Movement (music)business.industryrisk of injuryPhysical healthRisk factor (computing)preventionFMS textInjury riskMedicinerunnersbusinesshuman activitiesAmateurDemographyMedical Science Pulse
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Synergistic targeting of FLT3 mutations in AML via combined menin-MLL and FLT3 inhibition

2020

Abstract The interaction of menin (MEN1) and MLL (MLL1, KMT2A) is a dependency and provides a potential opportunity for treatment of NPM1-mutant (NPM1mut) and MLL-rearranged (MLL-r) leukemias. Concomitant activating driver mutations in the gene encoding the tyrosine kinase FLT3 occur in both leukemias and are particularly common in the NPM1mut subtype. In this study, transcriptional profiling after pharmacological inhibition of the menin-MLL complex revealed specific changes in gene expression, with downregulation of the MEIS1 transcription factor and its transcriptional target gene FLT3 being the most pronounced. Combining menin-MLL inhibition with specific small-molecule kinase inhibitors…

NPM1Transcription GeneticImmunologyApoptosisBiochemistryMiceRandom AllocationMice Inbred NODCell Line TumorProto-Oncogene Proteinshemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsGene expressionmedicineAnimalsHumansMEN1PhosphorylationMyeloid Ecotropic Viral Integration Site 1 ProteinProtein Kinase InhibitorsneoplasmsbiologyGene Expression Regulation LeukemicKinaseNuclear ProteinsMyeloid leukemiaDrug SynergismHistone-Lysine N-MethyltransferaseCell BiologyHematologymedicine.diseaseCoculture TechniquesNeoplasm ProteinsLeukemia Myeloid AcuteLeukemiaKMT2Afms-Like Tyrosine Kinase 3biology.proteinCancer researchNucleophosminProtein Processing Post-TranslationalTyrosine kinaseMyeloid-Lymphoid Leukemia ProteinBlood
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